There is increasing evidence from recent studies that a
large number of diseases are related to infections. In the
field of haematology, many malignant disorders are now
related to some infectious agents, such as Epstein-Barr
virus (EBV) in Burkitt's lymphoma, human T lymphocyte
virus I (HTLV-I) in T-cell leukaemia-lymphoma,
Helicobacter pylori in gastric B-cell lymphoma, human
herpes virus (HHV-6, -7, -8) in Kaposi's sarcoma and
Castelman's disease and, perhaps, parvovirus B19 in pure
red cell aplasia. However, all these infectious agents are
widespread in the general population, but only a very small
fraction of infected patients develop the neoplastic disease,
indicating the crucial role of some, at present unknown,
underlying genetic factors.
An association between HCV infection and B-cell
lymphoma has been demonstrated in several geographical
areas. Although controversy remains, a pathogenetic
linkage between HCV and NHL is strongly suggested by
molecular and epidemiological evidence. However, despite
this evidence, the pathogenetic mechanisms underlying
HCV-associated lymphomas are still unknown. HCV-related
lymphomas could, therefore, represent an important model
for analysing virus–induced lymphomas in humans.
It has not been elucidated whether HCV exerts its
oncogenic effect through an indirect mechanism or whether
it uses other pathways directly. It can be said that in most
cases the viral infection does not have a significant impact
on either response to chemotherapy or survival of
lymphoma patients. Chemotherapy is relatively safe and
treatment regimes do not usually need to be interrupted.
Since the treatment of HCV infection can lead to
regression not only of chromosomal and molecular
abnormalities, but even of clinically evident low-grade
NHL118.119, new therapeutic strategies (pegylated interferons
plus ribavirin), currently recognised as the gold standard
for HCV antiviral therapy and able to eradicate HCV in a
high percentage of treated subjects (from 60 to 90% of
complete responders on the basis of HCV genotype: 1 vs.
non-1) are likely to drastically reduce the number of HCV
infected patients and, consequently, the number of HCVrelated
NHL.
